36 results about "Long QT syndrome" patented technology

The invention provides a disposable sensor patch for the non-invasive detection of heart disease. The patch is placed on a person's chest area for automatic analysis of ECG. The heart condition is indicated via an indicator integrated within the patch. The patch is inexpensive and simple for self-administration. In one embodiment, the status of the heart is indicated via multiple LEDs. The detection and indication typically occurs, within 24 hours or sooner if a condition is readily identifiable. The patch is thin, flexible, and incorporates a battery, ECG amplifier, and a processor for analyzing ECG waveform and indicating the heart condition. A software algorithm searches for a cardiac abnormality such as arrhythmia, bradycardia, tachycardia, fibrillation, mycocardial infarction, ischemia, long-QT syndrome, blocks, late potentials, and premature contractions. In another embodiment, results and relevant ECG data are stored in memory for later retrieval.

A system for diagnosing Long QT Syndrome (LQTS) derives a QT / QS2 ratio from an electrical systole (QT) and a mechanical systole (QS2) to detect a prolonged QT interval in a patient's cardiac cycle. A processor acquires the systoles from a microphone and chest electrodes, calculates the QT / QS2 ratio, and outputs the result to a display. The processor may compare the QT / QS2 ratio to a threshold value stored in memory for diagnosing LQTS in the patient. A user interface provides for programming, set-up, and customizing the display. A mode selector allows the system to operate alternatively as a phonocardiograph, a 12 lead electrocardiograph, or a machine for diagnosing LQTS. A related method for diagnosing cardiac disorders such as LQTS includes measuring QT and QS2 during a same cardiac cycle, calculating a QT / QS2 ratio, and comparing the result to a threshold value derived from empirical data. The method may include measuring systoles both at rest and during exercise, and may be used for drug efficacy, dosage optimization, and acquired LQTS causality tests.

The present disclosure provides induced pluripotent stem (iPS) cells, and induced multipotent stem (iMS) cells, and progeny thereof, which cells include a gene encoding a polypeptide that regulates the QT interval. The present disclosure further provides panels of cardiomyocytes suitable for use in screening compounds for an effect on the QT interval. The cells and panels of cells can be used in a variety of applications, which are also provided.

A tolperisone-related compound or a compound of Formula Z is administered for the prevention and treatment of periodic paralyses and myotonias of several types, long QT syndrome, Brugada syndrome, malignant hyperthermia, myasthenia, epilepsy, ataxia, migraine, Alzheimer's Disease, Parkinson's Disease, schizophrenia, and hyperekplexia, neuropathic pain, and pain associated with nervous system disorders including, but not limited to, painful diabetic neuropathy, postherpetic neuralgia, trigeminal neuralgia, complex regional pain syndrome, Guillain-Barre syndrome (GBS), Charcot-Marie-Tooth (CMT) disease, complex regional pain syndrome, type 1 (CRPS-1), ischemic neuropathy, fibromyalgia, chronic fatigue syndrome, painful spasticities, and other nervous system disorders that have pain as an attendant sign and / or symptom.

The invention discloses a microRNA-328 and the application of antisense nucleotide thereof for diagnosing and controlling heart diseases; in the invention, a plurality of experiments prove that the microRNA-328 is changed and has pathopoiesia function in heavy heart diseases (atrial fibrillation, ischemia-reperfusion or myocardial fibrosis), and the antisense nucleotide AMO-328 of the microRNA-328has prevention and cure functions to the heart diseases, the microRNA-328 is used as a novel drug effect target spot, so as to finally determine and detect that the peripheral blood microRNA-328 canbe used as a novel biological marker which is used for diagnosing and preventing the heart diseases; in addition, the peripheral blood microRNA-328 expression level of a patient can be detected through fluorescent quantitative PCR and the nanometer microballoon technology enhanced by silver staining, so as to be used for diagnosing and preventing the heart diseases such as atrial fibrillation, long QT syndrome, ischemia-reperfusion or myocardial fibrosis and the like.

Provided are animal models of long QT syndrome (LQTS). The animal models are useful, for example, in screening of drugs for adverse effects in subjects with LQTS, in screening candidate therapeutics for the treatment or prevention of LQTS, and in determining gene expression in LQTS.

The present invention is directed to the use of Bortezomib and / or a pharmaceutically acceptable salt or ester thereof for the manufacture of a medicament for enhancing the expression of membrane proteins on the cell surface. Especially, the invention is directed to the use of Bortezomib for the manufacture of a medicament for the treatment of a disease of condition selected from the group consisting of cystic fibrosis, diabetes insipidus, hypercholesterinaemia and long QT-syndrome-2.

The present disclosure includes a system and method of detecting LQTS in a patient by comparing a collected set of ECG data from the patient to a plurality of databases of collected ECG data. The plurality of databases will include a database containing previous ECGs from the patient, a known acquired LQTS characteristics database, and a known genetic LQTS characteristics database. Comparing the patients ECG to these databases will facilitate the detection of such occurrences as changes in QT interval from success of ECGs, changes in T-wave morphology, changes in U-wave morphology and can match known genetic patterns of LQTS. The system and method is sensitive to patient gender and ethnicity, as these factors have been shown to effect LQTS, and is furthermore capable of matching a QT duration to a database of drug effects. The system and method is also easily integrated into current ECG management systems and storage devices.

The invention relates to a method for screening hERG potassium ion channel agonist and detecting toxicity. Particularly, the invention firstly relates to a fusion protein, which contains a fragment (which is used as the N end of the fusion protein, is from a position between 1st to 85th amino acid residues of the N end of the nemathelminth ERG family potassium ion channels UNC-103 protein and has the length of 75 to 85 amino acid residues), hERG or a fragment at least containing S1-S6 transmembrane domains and cyclic nucleotide binding domains, and a fragment (which is used as the C end of the fusion protein, is from a position between 590th to 829th of amino acid residues of the C end of the UNC-103 protein and has the length of 220 to 240 amino acid residues). The invention also relates to a polynucleotide sequence coding the fusion protein, a relevant transgenic nemathelminth, a relevant screening method and application. The inventor builds an in-vivo hERG-intracellular-transport-influence-recognizable compound molecule screening method for screening hERG inhibitors or LQTS (long QT syndrome) relevant channel mutant functional correcting agents for the first time; the novel path and method are provided for hERG toxicity detection and LQTS treatment medicine screening.

An ECG clock electrocardiogram based diagnostic device and method is disclosed. The ECG clock provides a clear visual indicator of heart related anomalies such as Long QT syndrome over a longer span of time than can otherwise be assimilated by a medical practitioner. A variable such as QT interval is represented by a variable length radial hand similar to a watch or clock hand. The circular face of the ECG clock represents the diagnostic time interval, typically 24 hours. The resulting output or plot of the ECG clock portrays a circular or polar mapping of the heart related variable such as QT interval over the diagnostic time interval, facilitating rapid diagnosis of volumes of electrocardiogram data by a medical practitioner that has heretofore not been possible.

The present disclosure relates to methods and compositions for modulating the activity of KCNQ channels as a means for reducing the effects of aberrant KCNQ channel function associated with epilepsy, deafness and arrhythmias including but not limited to, Long-QT syndrome (“LQTS”), and atrial fibrillation. The present disclosure also relates to the discovery of certain regions of KCNQ channels that interact with various channel stimulating molecules such as, ATP, and PIP2, as well as KCNQ channel domains that effect voltage dependant channel activation. The disclosure is also directed to the use of small molecules to modulate KCNQ channel activity in a cell. Moreover, the present disclosure relates to the therapeutic effects of treating a subject with modulators of KCNQ channel activity.

The invention relates to a method for detecting mutation of related genes of an genetic long QT syndrome, in particular relates to a method for detecting mutation of related genes, including KCNJ2 and CAV3, of the genetic long QT syndrome by combining a multi-oligonucleotide link detection probe with a liquid phase chip. The method comprises the following steps of: a) designing and preparing the multi-oligonucleotide link detection probe, wherein a probe sequence for mutation of the gene KCNJ2 is SEQ ID No.1-SEQ ID No.32, and the probe sequence for the mutation of the gene CAV3 is SEQ ID No.33-SEQ ID No.40; b) carrying out DNA sample denaturation and probe hybridization, and carrying out link reaction; c) carrying out PCR (polymerase chain reaction) amplification on the probe sequences by adopting a general primer; and d) detecting amplification products by utilizing the liquid phase chip. The technology can realize single-tube reaction detection on dozens of mutation sites at most, flux is high, operation is easy and cost is low.

The invention discloses an application of AMO-143 in preparation of a pharmaceutical composition for preventing and treating a long QT syndrome and promoting hERG expression, and the pharmaceutical composition for treating the long QT syndrome. The pharmaceutical composition is characterized by containing the AMO-143.

Provided are a model animal physiologically similar to humans, enabling a highly reproducible evaluation of the onset of drug-induced long QT syndrome, a method of generating the same, and an evaluating method using the same. A proarrhythmia model animal of a monkey, prepared by ablating the atrioventricular node; the foregoing monkey is preferably a cynomolgus monkey. A method of generating a proarrhythmia model animal, comprising a step for inserting an electrode catheter to the heart of a monkey, and ablating atrioventricular node with the catheter, and a method of evaluating the QT interval prolongation by a drug, comprising using the foregoing model animal.

The invention provides compounds which are selective PDE2 inhibitors for use in the treatment of tachycardia or tachyarrhythmia Such compounds are particularly suitable for use in the treatment of any of the following conditions: atrial tachycardia, atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia, premature ventricular contractions (PVCs), ventricular fibrillation and ventricular tachycardia, and may be used alone or in combination therapy with other conventional cardiovascular drugs, e.g. beta-blockers. In particular, the invention provides compounds which are selective PDE2 inhibitors for use in the treatment of ventricular tachycardia in patients who are suffering from, or who are at risk of suffering from heart failure, CPVT or long QT syndrome.

The invention relates to the technical field of human genetics and internal medicine cardiovascular systems, in particular to a KCNH2 mutant gene; wherein in the genome position chr7: 150654492, a basic group A is mutated into a basic group T, and the reference genome version is GRCh37. The invention also relates to a long QT syndrome detection kit, which comprises a forward primer and a reverse primer designed according to the KCNH2 mutant gene, the sequence of the forward primer is SEQ ID NO: 5, and the sequence of the reverse primer is SEQ ID NO: 6. The human KCNH2 mutant gene provided by the invention can be used for distinguishing long QT syndrome patients from normal people and is used as a biomarker for clinical auxiliary diagnosis of the long QT syndrome; by detecting a carrier of the variation, prenatal guidance and genetic counseling can be provided for a subject, and birth of a child patient is reduced; according to the invention, a possible drug target is provided for human to treat the long QT syndrome, and research and development of innovative drugs are promoted.

The present disclosure provides, inter alia, a recombinant engineered deubiquitinase (DUB) and methods for treating or ameliorating an inherited ion channelopathy, such as long QT syndrome, Brugada syndrome, or cystic fibrosis, in a subject. Further provided are methods for screening mutations causing such inherited ion channelopathies for a trafficking-deficient mutation that is treatable by the recombinant engineered DUB disclosed herein.

The invention belongs to the field of animal experiment modeling methods, and relates to a polypeptide for constructing a long QT syndrome animal model and a method for establishing an animal model for an animal experiment. According to the polypeptide for constructing the long QT syndrome animal model, an amino acid sequence of the polypeptide is GRKKRRQRRRGEVDEMIREADIDGDGQVNYEGFVQMM, and the polypeptide is named as CM4. The method for establishing the long QT syndrome animal model comprises the step of administering the polypeptide CM4 to an animal to obtain the long QT syndrome animal model. The model establishing method provided by the invention is simple and reliable, and is convenient for researchers to establish a long QT syndrome mouse or guinea pig isolated heart model and carry out related experimental researches. The modeling process is simple and effective, meanwhile, a corresponding control group can be set, and electrocardiogram changes before and after amino acid mutation are compared and analyzed. The CM4 is given to induce the QT interval of isolated hearts of mice and guinea pigs to be prolonged, the CM4 is easy to obtain and high in purity, the CM4 can penetratethrough cell membranes to enter cells to play a role, the activity of myocardial calcium channels is adjusted, the molding efficiency is high, the cost is low, and research of related experiments is facilitated.

The present invention is directed to the use of a compound stimulating deubiquitinating activity in a cell for the manufacture of a medicament for enhancing the expression of integral membrane proteins on the cell surface. Especially, the invention is directed to the use of such compound for the manufacture of a medicament for the treatment of a disease of condition selected from the group consisting of cystic fibrosis, diabetes insipidus, hypercholesterinaemia and long QT-syndrome-2.

The present invention relates to generating hiPSC-derived cardiomyocytes and embryoid bodies that recapitulate the disease phenotype of Long QT Syndrome and their use in developing pharmacological treatments thereof. The present invention also includes the use of a compound which inhibits the ubiquitin-proteasome pathway for the preparation of a medicament for the prophylaxis or treatment of a disease associated with prolonged ventricular repolarization (cardiac arrhythmia) caused by one or more mutations in the amino acid sequence of the hERG potassium channel.

The invention discloses a molecular marker capable of prognosing long QT syndrome (LQTs) attack risks and diagnosing the LQTs, namely miRNA (microribonucleic acid)-3619, and an application of antisense oligonucleotides AMO-3619 of miRNA-3619 in preparation of medicines for treating the LQTs, mainly an application of the medicines in promotion of human ether-a-Go-Go related gene (hERG) functions. The molecular marker is characterized in that the medicine composition contains AMO-3619.

The invention discloses an LQTS patient self-management method and device, electronic equipment and a storage medium. The method comprises the steps: obtaining the registration information of a current LQTS patient; identifying risk stratification of the current LQTS patient according to the registration information, and determining matters needing attention of the current LQTS patient; and when the matters needing attention are reminded, generating medicine query information corresponding to at least one evaluation in the evaluation result. The functions of the embodiment of the invention comprise risk hierarchical self-evaluation, diet guidance, medication guidance, exercise guidance, special matters needing attention and the like, and the awareness rate of the sudden death risk of the patient with the long QT syndrome is improved through an informatization means, so that the sudden death risk of the patient is reduced, the life of the patient is prolonged, the life quality is improved, and the family burden is relieved.